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Enzyme Catalysis
Published in Harvey W. Blanch, Douglas S. Clark, Biochemical Engineering, 1997
Harvey W. Blanch, Douglas S. Clark
The first cytokine approved for clinical use was interferon- α in 1986 . There are three types of interferons, IFN- α, IFN- β and IFN- γ. When a virus attacks a cell, it may produce and release interferons. The interferon then induces other cells to become resistant to the virus. Treatment with IFN may be effective with established viral infections, such as hepatitis B and genital warts. Recombinant IFN- α or lymphoblastoid interferon is produced in E. coli, as the unglycosylated form of IFN- α retains its biological activity. IFN- β or fibroblast interferon was produced in fibroblasts exposed to viruses. It can now be produced in E. coli, yeast and CHO cells, as can IFN- γ, although most emphasis on commercial production centers on recombinant E. coli. The interferons are purified from cell homogenates by affinity chromatography (using lectins, anti-IFN MAbs, or concanavalin A as ligands), ion exchange and HPLC.
Cyclopolymerization of Dienes with Selected Vinyl Monomers
Published in George B. Butler, Cyclopolymerization and Cyclocopolymerization, 2020
Interferon, first discovered in 1957,118 is a substance of protein-like structure that is produced in the cells of vertebrates in response to viral infection, and possesses antiviral action. Today, it is generally accepted that interferon plays an essential role in the formation of a host’s nonspecific resistance to super-infection with a second virus.119 Thus, the role of interferon in combating viral infections may be similar to that of antibodies toward bacterial infections. It is immediately apparent that a successful and readily available interferon inducer, such as DIVEMA, could play an extremely significant role not only in aiding recovery from a viral infection, but also in its use in a prior generation of interferon to prevent a viral attack.
Biochemical Indices of Fatigue for Anti-fatigue Strategies and Products
Published in Gerald Matthews, Paula A. Desmond, Catherine Neubauer, P.A. Hancock, The Handbook of Operator Fatigue, 2017
Yasuyoshi Watanabe, Hirohiko Kuratsune, Osami Kajimoto
A rather different perspective on fatigue comes from studies of the immune system, which protects the body against infections caused by viruses and bacteria. The importance of the immune system is suggested by observations that chronic fatigue may follow viral infection, or a past history of allergies. Substances known as cytokines (e.g., interferon) regulate the activity of the immune system, either stimulating or suppressing immune response. Broadly, prolonged activation of the immune system may be linked to chronic fatigue. In section 6, we examine abnormalities in some of the specific biochemical pathways that have been implicated in fatigue.
Soluble expression, rapid purification, biological identification of chicken interferon-alpha using a thioredoxin fusion system in E. coli and its antiviral effects to H9N2 avian influenza virus
Published in Preparative Biochemistry and Biotechnology, 2019
Jun Zhao, Hai-Yang Yu, Yu Zhao, Feng-Hua Li, Wei Zhou, Bin-Bin Xia, Zhi-Yuan He, Jason Chen, Guo-Tuo Jiang, Ming-Li Wang
Interferons (IFNs) are a large family of cellular glycoproteins that are produced by immune cells and have anti-tumoral, antiviral, and immunomodulatory functions.[1] Among them, chicken interferon-α (ChIFN-α) belongs to type I IFNs and is essential for activating host immune responses against virus infections.[2] To date, chicken interferon-α (ChIFN-α) has been recorded as a powerful antiviral agent in responding to infections induced by Newcastle disease virus (NDV),[3] infectious bronchitis virus,[4] infectious bursal disease virus,[5] Marek’s disease virus,[6] Rous sarcoma virus,[7] and influenza viruses, such as the Avian influenza A/H9N2 virus.[8,9] Moreover, the adjuvant function of rChIFN-α was proved in various models of infection,[10] suggesting the future prospect of rChIFN-α being used for the control of chicken virus infections.
Evaluation of a single amino acid substitution at position 79 of human IFN-α2b in interferon-receptor assembly and activity
Published in Preparative Biochemistry and Biotechnology, 2019
Samira Talebi, Alireza Saeedinia, Mehdi Zeinoddini, Fathollah Ahmadpour, Majid Sadeghizadeh
Human interferon-α (IFN-α) is a member of the type I interferon (IFN-I) that are commonly recognized to prompt a potent innate immune response in contradiction of both cancers and viral infection.[18–20] IFN-α has been regularly used as an informing mediator for the treatment of several malignancies like renal cell cancer, hepatocellular carcinoma, and malignant melanoma by motivating of tumor cells apoptosis. Moreover, the effect of IFNα on cervical cancer has been studied by Shi et al. 2016.[21] HeLa cells were used as a testing model for the treatment of IFN-α on cervical cancer. The results show that IFNα prominently prevents the proliferation and prompts the HeLa cells apoptosis.
Nanomaterials against pathogenic viruses: greener and sustainable approaches
Published in Inorganic and Nano-Metal Chemistry, 2020
Ghazaleh Jamalipour Soufi, Siavash Iravani
A one-step approach was applied for synthesis of cationic carbon dots form curcumin with antiviral characteristics.[56] It was observed that carbon dots inhibited the proliferation of PEDV (as a model of CoVs; an alpha-CoV), and changed the structure of surface protein in viruses, thus avoiding the entrance of viruses. Cationic carbon dots based on curcumin suppressed the formation of negative-strand RNA and budding of the virus and the accumulation of reactive oxygen species by virus. Further, it suppressed the viral replication by stimulating the generation of interferon-stimulating genes (ISGs) and pro-inflammatory cytokines.[56] In an interesting study, the antiviral activities of seven different carbon quantum dots for treating human CoV HCoV-229E contagions were evaluated. The carbon quantum dots (∼10 nm, high solubility in water) were fabricated for concentration-dependent virus inactivation (EC50 = 52 ± 8 μg/mL).[57] Further, carbon quantum dots (EC50 = 5.2 ± 0.7 μg/mL) were fabricated for inhibition of HCoV-229E entrance, which is probably because of the functional groups interaction of the quantum dots with entry receptors of the virus. The viral replication step also demonstrated a similarly big inhibition activity.[57] Moreover, polyamine carbon quantum dots attached to white spot syndrome virus (WSSV) envelope and inhibited the virus infection, with a dose-dependent influence.[48] It was demonstrated that the prepared quantum dots upregulated several immune genes in shrimp and reduced the mortality upon this viral infection (Figure 5).[48]